Effect of heat stress on vascular outcomes in humans

Abstract

In addition to its role as an environmental stressor, scientists have recently demonstrated the potential for heat to be a therapy for improving or mitigating declines in arterial health. Many studies at both ends of the scientific controls spectrum (tightly controlled, experimental vs. practical) have demonstrated the beneficial effects of heating on microvascular function (e.g., reactive hyperemia, cutaneous vascular conductance); endothelial function (e.g., flow-mediated dilation); and arterial stiffness (e.g., pulse-wave velocity, compliance, β-stiffness index). It is important to note that findings of beneficial effects are not unanimous, likely owing to the varied methodology in both heating protocols and assessments of outcome measures. Mechanisms of action for the effects of both acute and chronic heating are also understudied. Heat science is a very promising area of human physiology research, as it has the potential to contribute to approaches addressing the global cardiovascular disease burden, particularly in aging and at risk populations, and those for whom exercise is not feasible or recommended.

Keywords: arterial stiffness; endothelial function; heat stress; heat therapy; vascular physiology.

Fig. 1.

Assessment methods for common vascular structure and function outcomes. Structural and functional characteristics are typically assessed at the common carotid artery (CCA), brachial artery (BA), superficial femoral artery (SFA), and the microvasculature. Microvascular function can be assessed through cutaneous vascular conductance (CVC) or reactive hyperemia (RH) response. Endothelial function can be assessed through flow-mediated dilation (FMD). Arterial stiffness can be assessed locally through compliance, distensibility, and the β-stiffness index, or regionally through pulse-wave velocity (PWV) at a variety of arterial sites. Arterial intima-media thickness (IMT) describes the thickness of the arterial wall, most typically at the CCA, and is a precursor to atherosclerosis.

Fig. 2.

Blood flow distribution at rest and during heat stress. During whole-body heat stress, cardiac output (CO) increases from ~5 to 12.5 l/min, a 2.5-fold increase. Blood flow is redirected to the skin (↑ 7–8 l/min) (39) from the splanchnic (↓ 40%) (61) and renal (↓ 15–30%) (72) regions, such that the organs comprise ~60, 5–6, and 6–7% of cardiac output with heating, respectively. Gray circles indicate the percent contribution to CO at rest, blue circles indicate a decrease in percent contribution to CO during heat stress, and red circles indicate an increase in percent contribution to CO during heat stress. Illustrations of human body organs produced by Servier Medical Art.

Fig. 3.

Potential control mechanisms for the effect of heat stress on the vasculature. Heat stress can be characterized by frequency, temperature, mode, localization, and duration, to determine the magnitude and intensity of the stimulus. Heat alters vascular shear stress, heat shock protein content, autonomic nervous system activity, endothelial cell damage pathways, and inflammation and oxidative stress, all of which are associated with the regulation of secreted vasoactive substances to mediate arterial adaptation.